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Gastroenterology - Esophageal Disorders and Gastroesophageal Reflux Disease - Fast Facts | NEJM Resident 360

Patients with esophageal disorders often present with difficulty swallowing or dysphagia, typically related to a structural or motility abnormality. Generally, patients present to the outpatient clinic, although inpatient admissions may occur in some cases (e.g., food-bolus obstruction).

• Oropharyngeal****dysphagia (or transfer dysphagia) is characterized by difficulty in initiating a swallow and often presents with drooling, coughing related to aspiration, and sialorrhea.

• Esophageal****dysphagia is experienced as the sensation of food going down slowly or getting stuck in the chest at least several seconds after initiating a swallow.

However, where the patient localizes the dysphagia is not always a good predictor of the location of the problem (for example, an obstruction at the lower esophageal sphincter may be experienced as dysphagia in the upper chest).

Esophageal Dysphagia: The causes of esophageal dysphagia can be categorized as structural disorders or motility disorders.

• Structural disorders include the following:

  • intrinsic esophageal obstruction

    • strictures related to esophagitis or malignancy

  • extrinsic esophageal stricture

    • vascular anomaly

    • malignancy/mass in chest or mediastinum

  • esophageal rings and webs

    • Plummer–Vinson syndrome (esophageal ring)

    • Schatzki ring

  • food impaction

• Motility disorders can be categorized as primary and secondary esophageal motility disorders as defined in the following table.

(Source: Esophageal Motility Disorders and Gastroesophageal Reflux Disease. N Engl J Med 2020.)

In this section, we review the following common esophageal disorders:

• gastroesophageal reflux disease (GERD)

• eosinophilic esophagitis

• achalasia

Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) is the second most common gastrointestinal diagnosis in the ambulatory setting and affects 18%–28% of people living in the North America. It is caused by transient relaxation of the lower esophageal sphincter (LES), which allows acidic stomach contents to reflux into the esophagus.

Presentation

Patients with GERD often present with heartburn, regurgitation, mild dysphagia, and noncardiac chest pain. Upper airway symptoms of cough, throat clearing, and hoarseness are also common. Diagnostically, symptom response to a 6-week course of once-daily proton pump inhibitor (PPI) therapy confirms the clinical diagnosis in patients with typical symptoms. Patients with alarm symptoms (e.g., severe or worsening dysphagia, weight loss, or iron deficiency anemia) should first undergo endoscopic evaluation.

Management

• Histamine-2 (H₂) blocker or proton pump inhibitor (PPI): Management of GERD includes inhibition of gastric acid secretion with either an H₂ blocker or PPI. PPIs must be taken 30 to 60 minutes before a meal and are most effective when taken on an empty stomach. First-line treatment is 4–8 weeks of an H₂ blocker or PPI followed by a taper to the lowest dose of acid suppression needed for symptom control. Further testing and acid inhibition therapy is indicated for patients with persistent symptoms following 6–8 weeks of therapy. 

• Recommended lifestyle measures include avoiding trigger foods (e.g., chocolate, spicy meals, coffee, acidic drinks, large fatty meals), avoiding food within 3 hours of bedtime, weight loss, smoking cessation, and sleeping with the head of the bed raised.

• Antireflux surgery (e.g., fundoplication or LINX device) is generally reserved for patients with GERD that is refractory to intensive medical therapy.

Barrett Esophagus

Barrett esophagus is the asymptomatic replacement of the normal squamous epithelium of the esophagus by metaplastic columnar epithelium caused by chronic esophageal inflammation secondary to acid reflux. Barrett esophagus is a rare but important precursor for esophageal adenocarcinoma.

Screening for Barrett esophagus by endoscopic evaluation should be considered in men with chronic and/or frequent symptoms of gastroesophageal reflux and risk factors (including age, presence of obesity, smoking, or family history). Screening in women and the general population is not recommended.

Diagnosis of Barrett esophagus is confirmed by targeted and random biopsies throughout the length of the esophagus to identify intestinal metaplasia with goblet cells. These changes are highlighted in the following diagram:

Diagnostic Features of Barrett Esophagus

The diagnosis of Barrett esophagus requires endoscopic evidence that columnar mucosa extends above the gastroesophageal junction and lines the distal esophagus, plus esophageal-biopsy results that confirm the presence of columnar metaplasia. Endoscopically, the gastroesophageal junction is identified as the most proximal extent of the gastric folds (dashed white line). Salmon-colored columnar mucosa extends in tongue-shaped projections above the gastroesophageal junction, lining the distal esophagus. A biopsy specimen obtained at the level of the upper white dot reveals the junction between esophageal stratified squamous epithelium and intestinal metaplasia with distinctive, intestinal-type goblet cells, which establishes the diagnosis of Barrett esophagus. Intestinal metaplasia may not be uniformly distributed throughout the entire columnar-lined esophagus, however. In this example, a biopsy specimen taken from the columnar-lined esophagus closer to the gastroesophageal junction (at the level of the lower white dot) shows cardiac mucosa composed of mucus-secreting columnar cells without goblet cells.
(Source: Barrett’s Esophagus. N Engl J Med 2014.)

Surveillance: Regular surveillance with endoscopy according to the following recommendations are important for assessing potential malignant transformation. The screening interval depends on the level of dysplasia. Patients with high-grade dysplasia are considered for surgery or endoscopic mucosal ablation or resection.

• no dysplasia: follow-up endoscopy every 3–5 years

• low-grade dysplasia: endoscopy every 6–12 months until dysplasia is absent on two consecutive examinations

• high-grade dysplasia: surgery or endoscopic mucosal ablation or resection, followed by endoscopic surveillance every 3 months for one year before lengthening surveillance duration if dysplastic changes are absent on two consecutive examinations

Acid inhibitor therapy is recommended for all patients with Barrett’s esophagus irrespective of reflux symptoms

Eosinophilic Esophagitis

Eosinophilic esophagitis (EoE) is a chronic, allergen-driven, immune-mediated disease that has increasingly been recognized as a cause for dysphagia and food-bolus impaction. EoE is often associated with atopy, asthma, and other allergic manifestations outside of the gastrointestinal tract. A clue to EoE is burning, itching, or tingling of the lips, mouth, and throat when the trigger food is ingested. The incidence and prevalence of EoE has increased significantly during the past few decades.

Diagnosis

Diagnosis of EoE requires an esophageal biopsy showing infiltration of eosinophils of at least 15 eosinophils per high-power microscopy field. A characteristic finding of EoE on endoscopy is “trachealization” of the esophagus, or circular rings that contribute to dysphagia. Note that GERD and PPI-responsive esophageal eosinophilia can also cause similar findings and must be ruled out before a diagnosis of EoE is made.

“Trachealization” of the Esophagus

Upper endoscopy revealed prominent mucosal rings extending 20 cm from the incisors to the level of the gastroesophageal junction, with two discrete areas of narrowing and associated linear furrows.
(Source: “Trachealization” of the Esophagus. N Engl J Med 2019.)

Management

Treatment of EoE includes PPIs, trial of an elimination diet to remove potential allergens, and swallowed topical glucocorticoids. Mechanical dilatation may also be required if there is evidence of esophageal narrowing. The following table summarizes medical treatment options for EoE in further detail:

(Source: Eosinophilic Esophagitis. N Engl J Med 2015.)

Achalasia

Achalasia is a rare motility disorder characterized by impaired relaxation of the lower esophageal sphincter (LES) and failure of the esophageal smooth muscle to produce adequate peristalsis. Clinically, patients report dysphagia of solids and liquids, regurgitation, nocturnal cough, chest pain, heartburn, and weight loss.

Diagnosis

• Manometry is the most sensitive test for the diagnosis of achalasia. The classic manometric findings are diminished or absent primary peristalsis, increased resting LES pressure, and impaired LES relaxation during a test swallow.

• CT can be used to rule out pseudoachalasia caused by gastric or intrathoracic malignancy.

• Endoscopy is required to exclude malignancy and other causes of dysphagia.

• Barium esophagram can also assist in diagnosis. The classic appearance consists of a dilated esophageal body, and a tapered “bird’s beak appearance,” as shown in the following image:

Typical “Bird’s Beak Appearance” of Achalasia

A barium-swallow study showed a dilated esophagus (long arrow) with tapering at the distal end (short arrow). This tapering is often referred to as “bird’s beak appearance” and is typical of achalasia.
(Source: Achalasia. N Engl J Med 2012.)

Treatment

Treatment of achalasia is aimed at reducing the high pressure in the LES, either via endoscopy or surgery with the modalities outlined in the following table:

Treatment Options for Achalasia
Endoscopic

• Pneumatic balloon dilatation

• Botulinum toxin injections

• Peroral endoscopic myotomy (POEM)

| | Surgical |

• Heller myotomy

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